Influenza Virus Assembly and Budding
By Jeremy S. Rossman, R. Lamb. Virology, 2011
691 citations recorded by the source corpus.
Influenza A virus causes seasonal epidemics, sporadic pandemics and is a significant global heath burden. Influenza virus is an enveloped virus that contains a segmented negative strand RNA genome. Assembly and budding of progeny influenza virions is a complex, multistep process that occurs in lipid raft domains on the apical membrane of infected cells. The viral proteins hemagglutinin (HA) and neuraminidase (NA) are targeted to lipid rafts, causing the coalescence and enlargement of the raft domains. This clustering of HA and NA may cause a deformation of the membrane and the initiation of the virus budding event. M1 is then thought to bind to the cytoplasmic tails of HA and NA where it can then polymerize and form the interior structure of the emerging virion. M1, bound to the cytoplasmic tails of HA and NA, additionally serves as a docking site for the recruitment of the viral RNPs and may mediate the recruitment of M2 to the site of virus budding. M2 initially stabilizes the site of budding, possibly enabling the polymerization of the matrix protein and the formation of filamentous virions. Subsequently, M2 is able to alter membrane curvature at the neck of the budding virus, causing membrane scission and the release of the progeny virion. This review investigates the latest research on influenza virus budding in an attempt to provide a step-by-step analysis of the assembly and budding processes for influenza viruses.
Subfields: Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6c9bcc7804743feed8349eab3ed8ccd04f319271
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In Epidemiology
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Citations in the corpus
- Meta- and Orthogonal Integration of Influenza “OMICs” Data Defines a Role for UBR4 in Virus Budding (2015, background): “UBR4 Interacts with the M2 Ion Channel and Is Required for IAV Replication M2 is an ion channel protein that plays crucial roles during IAV entry and exit (Edinger et al., 2014; Rossman and Lamb, 2011).”